[Fatty acid composition of the plaques of demyelination in multiple sclerosis].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to L Amaducci.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
This is the first report of the presence of free D-amino acids in lumbar and ventricular human cerebrospinal fluid (CSF) of individuals with Alzheimer disease (AD) compared with CSF of normal control subjects and with individuals affected by multiple sclerosis, as an unrelated neurologic disorder. Free D-amino acids are present at significantly higher levels in AD CSF than normal CSF, whereas in the CSF of patients affected by multiple sclerosis, D-amino acids occurs at the same level as in the normal controls. The total D-amino acid content in ventricular CSF was 1.48 times higher in the AD than controls (26.4 vs 17.9 nmol/mL, p = 0.025). The total D-amino acid content was 1.43 times higher in AD lumbar CSF than controls (1.89 vs 1.32 nmol/mL, p = 0.001). D-Aspartate in particular was 2.74 times higher in AD ventricular CSF compared to normal ventricular CSF (3.34 vs 1.22 nmol/mL, p = 0.029). In lumbar CSF, D-aspartate was 1.5 times higher in AD than controls (0.054 vs 0.036 nmol/mL, p = 0.041). Previously we reported that D-amino acids are elevated in AD brain proteins associated with neurofibrillary tangles compared to normal brain proteins (D'Aniello et al., 1992c; Fisher et al., 1992a,b). Thus, the D-amino acids present in CSF may originate from degradation of brain proteins.
Putative risk factors for Alzheimer's disease, other than familial aggregation, are: Down's syndrome among relatives, late maternal age, head injury, viral agents, toxic exposures, and immune factors. Current epidemiologic and genetic data are inconclusive, but indicate etiologic heterogeneity. We suggest to investigate separately: autosomal dominant, familial, and sporadic cases.
Human diploid fibroblasts undergo replicative senescence in vitro, which is strongly correlated with biological aging in vivo. In order to examine whether features compatible with a systemic premature aging are present in familial Alzheimer's disease (FAD) patients, we investigated the growth characteristics of three skin fibroblast lines from FAD patients and from three sex/age-matched controls at different passages until senescence was reached. A kinetic study of the replicative capacity was performed at different culture times by [3H]-thymidine incorporation and crystal violet staining. Data showed no significant difference between the two groups at any studied passage. The life span of the two types of cultures was also comparable. These results suggest that in familial Alzheimer patients there are not systemic signs of accelerated aging.
We sought to identify the most reliable magnetic resonance (MR) measures for the diagnosis and staging of Alzheimer disease (AD) in a clinical setting and to estimate, for different degrees of dementia, the rate of change of cerebral atrophy in certain regions of interest (ROIs). Forty-two probable AD patients and eight normal controls underwent MR brain scans, neurological examinations, and neuropsychological testing. We computed each subject's corpus callosum width, ventricular size, right and left temporal lobe areas, interuncal distance, and assessed the degree of cortical atrophy. We also estimated the rate of change for Information-Memory-Concentration Test scores and for temporal lobe areas and corpus callosum width. Measures of temporal lobe area and subjective evaluation of temporal lobe atrophy both served to distinguish controls from mild AD cases (p < 0.05), whereas only the latter differentiated moderate from severe patients (p < 0.05). The rate of change for temporal lobe areas remained constant over different AD stages, whereas those for corpus callosum width and for cognitive impairment were greater for severe cases (p < 0.05). Our findings imply that measurements of temporal lobe area and ratings of temporoparietal atrophy can be useful in the diagnosis and staging of AD and suggest that atrophy progressed at different rates in selected ROIs for various stages of AD severity.
Stroke prevalence surveys are more and more needed for health care and facility planning. Prevalence estimates and costs of the definition procedure may vary depending on different screening strategies. We evaluated the impact of these different strategies on the overall diagnostic procedure and on stroke prevalence estimates in the Italian Longitudinal Study on Aging. A population sample of 5, 632 individuals aged 65-84 years was screened for stroke by a simple question on previous stroke diagnosis, questions on possible stroke symptoms and a simple neurological examination. Those screened positive by any of these procedures were fully examined by a neurologist for conclusive diagnosis. We determined the positive predictive value of each procedure on the final stroke diagnosis and calculated prevalence as if each procedure had been used separately. Using the three procedures combined, the prevalence rate was 6.0% (95% confidence interval, 5.4-6.7%). If each procedure had been used as the unique screening tool, the rates would have been 5.1% (4.5-5. 7%), 4.1% (3.6-4.7%) and 2.3% (1.9-2.7%), and positive predictive values 66.4, 55.2 and 45.1%, respectively. Different screening procedures can affect stroke prevalence estimates. Compared to more complex screening strategies, the use of a simple question about previous diagnosis as the unique screening tool leads to only a slight underestimation of stroke prevalence and avoids a 66% increase in the number of subjects to be examined in a second-level specialist evaluation, potentially reducing the costs of the overall diagnostic procedure.
Owing to the involvement of Italian Centres in a multicentre, German-Italian therapeutical trial with Alzheimer's dementia patients, to be assessed with the Alzheimer's Disease Assessment Scale (ADAS), it was decided that the Italian centres would use an Italian version of the scale, derived from that used by the German centres. However, the lists of words for exploring verbal memory are not merely translated from the German version, but are composed of selective Italian words chosen according to linguistic criteria. This Italian version was validated following the same procedure adopted for validating the German version. We submitted this Italian version to an interrater reliability, test-retest reliability, concurrent validity, internal consistency and sensitivity evaluation, using demented patients. Based on the results of these tests this Italian version of the ADAS proved valid and reliable. Moreover, the results were strikingly comparable to those from the validation of the German version. Our work supports the validity, reliability and transnational comparability of national versions of the ADAS constructed following definite linguistic criteria.
Explore the source record for details and available documents.
Previous studies on the clinical features of meningoencephalitis in Italy did not help to indicate the nature of the causative agents. On the other hand during the past decade nine arboviruses were isolated in Italy, some of which are yet to prove pathogenic for man. A systematic study was carried out in cooperation between the Department of Neurology of the University of Florence and the Istituto Superiore di Sanità (Rome), in order to understand a possible role of arboviruses as etiologic agents of meningoencephalitis in Italy; in this preliminary communication the first clinical case of Tick-Borne Encephalitis (TBE) virus infection is described.
Statistics indicate that in Europe people over 65 years of age will be 23.5% at the beginning of the next century and prevalence of severe dementias is estimated to be 5% in this population group. Clinically, dementia is a syndrome characterized by memory loss, other cognitive dysfunctions and loss of ability for self-care. This organic syndrome, that can have many different causes, must be differentiated from other similar psychiatric disorders of the elderly such as the pseudo-dementias. The most important of these causes are Alzheimer's disease (AD) and vascular dementias. Other causes are infections, toxic and metabolic disorders, normal pressure hydrocephalus and head trauma. Many efforts are required in order to reach an accurate differential diagnosis, as 10-15% of the dementia syndromes are reversible if an appropriate therapy is applied. Because of its high frequency, AD is one of the most actively studied areas in dementia research. The specific causes of AD are still unknown, but recent case-control studies suggest the importance of risk factors such as familiarity and previous head trauma. Other hypotheses concern prion infections, aluminium toxicity and immunologic disorders. The most important findings of the last years however, concern biochemical alterations in Alzheimer's brains. After the first observations of Davies and Maloney (1976), who observed a reduction of choline acetyltransferase in cerebral cortex, many reports successively indicated the importance of deficiencies of the cholinergic systems in AD. Other neurotransmitter systems, such as the noradrenergic and the serotoninergic systems, were also found to be involved in AD. From these findings a rational therapeutic approach to the disease was proposed. Initially, the clinical trials employed physostigmin with uncertain results. Later, therapeutic attempts with choline, lecitine, acetylcarnitine and phosphatidilserine resulted more promising, at least in the initial phase. However, consistent data are not yet completely available. Finally, the management of AD also concerns problems of familiar education to the behavioural management of AD patients and the eventual possibilities of social assistance. Vascular dementia and Creutzfeldt-Jakob disease will also be discussed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Two form of retinoic acid (RA) prevented the development of experimental allergic encephalomyelitis (EAE) in Lewis rats. RA suspended in corn oil was given before the expected onset of the disease to rats immunized with myelin and to controls. The drug suppressed the neurological symptoms as well as the perivascular infiltrates observed in vehicle treated animals. The results indicate that, under these experimental conditions, RA has immunosuppressive activity by interfering with the efferent phase of the immune response.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.